Dr. Jeffrey M. Dodd-o is an associate professor of anesthesiology and critical care medicine at the Johns Hopkins University School of Medicine. He has a secondary appointment in surgery. His area of clinical expertise is cardiac anesthesiology.

Dr. Dodd-o received undergraduate degrees in general arts and sciences and Spanish from Pennsylvania State University. He earned his medical degree from the Medical College of Pennsylvania, followed by an internship in general surgery at Northeastern Ohio University’s Youngstown Hospital, and a Ph.D. in physiology from the University of North Texas. He then completed a residency in anesthesiology and performed a fellowship in critical care medicine at the Johns Hopkins University School of Medicine. Dr. Dodd-o joined the Johns Hopkins faculty in 1994.

He is a diplomate of the American Society of Anesthesiologists and holds a special certificate of competency in critical care medicine.

His research focuses on understanding the factors that contribute to ischemia and reperfusion injury of the lung and how ischemia and reperfusion contribute to lung dysfunction in the early post-cardiopulmonary bypass period.

Dr. Dodd-o’s experiences as a cardiac anesthesiologist and his work with heart and lung transplantation patients in the cardiac surgical intensive care unit led him to his chosen path of scientific investigation. His principle research efforts are engaged in understanding the factors that contribute to ischemia/reperfusion injury of the lung and the contribution of ischemia/reperfusion to the lung dysfunction seen in patients in the early post-cardiopulmonary bypass period. To this end, he has developed a sensitive model of ischemia/reperfusion in a spontaneously breathing mouse. He is using this model and an in situ mouse lung preparation to identify cardiopulmonary interactions that affect lung injury caused by reperfusion. As an example, Dr. Dodd-o and his colleagues are attempting to characterize the influence on lung microvascular permeability of atrial natriuretic peptide (ANP), which is secreted by the heart. Their preliminary observations indicate that ANP is sometimes injurious and sometimes protective to the lung, and they are working to determine the factors that alter its influence on lung permeability.

In another area of study, Dr. Dodd-o is utilizing various preclinical models to begin to explore the influences of mechanical ventilation on lung injury and kidney function, as well as the interaction of mechanical ventilation and kidney injury on lung function.

Dr. Dodd-o’s long-term goal is to use a mouse lung transplantation model to distinguish immunologic effects from reperfusion effects on graft survival. Lung inflammation can be caused by rejection; it can also be caused by reperfusion. With models of both, Dr. Dodd-o hopes to distinguish which aspects of lung injury following transplantation are due to reperfusion and which are immunologically mediated.

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Selected Publications

  1. Li D, Fernandez LG, Dodd-o J, Langer J, Wang D, Laubach VE. Upregulation of hypoxia-induced mitogenic factor in compensatory lung growth after pneumonectomy. Am J Respir Cell Mol Biol 32(3):185–91, 2005.
  2. Tong Q, Zheng L, Kang Q, Dodd-o J, Langer J, Li B, Wang D, Li D. Upregulation of hypoxia-induced mitogenic factor in bacterial lipopolysaccharide-induced acute lung injury. FEBS Lett 17;580(9):2207–15, 2006.
  3. Dodd-o JM, Hristopoulos ML, Welsh-Servinsky LE, Tankersley CG, Pearse DB. Strain-specific differences in sensitivity to ischemia-reperfusion lung injury in mice. J Appl Physiol 100(5):1590–5, 2006.
  4. Papaiahgari S, Yerrapureddy A, Reddy SR, Reddy NM, Dodd-o JM, Crow MT, Grigoryev DN, Barnes K, Tuder RM, Yamamoto M, Kensler TW, Biswal S, Mitzner W, Hassoun PM, Reddy SP. Genetic and pharmacologic evidence links oxidative stress to ventilator-induced lung injury in mice. Am J Respir Crit Care Med 176(12):1222–35, 2007.
  5. Dodd-o JM, Hristopoulos ML, Kibler K, Gutkowska J, Mukaddam-Daher S, Gonzalez A, Welsh-Servinsky LE, Pearse DB. The role of natriuretic peptide receptor-A signaling in unilateral lung ischemia-reperfusion injury in the intact mouse. Am J Physiol Lung Cell Mol Physiol 294(4)L714–23, 2008.


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